Cytochemistry of Hippocampus Following Cerebral Ischemia

  • B. J. Mršulja
  • M. Spatz
  • I. Klatzo

Abstract

The feature of selective vulnerability to ischemia displayed by certain topistic units and most clearly observed in the hippocampus, the brain region particularly sensitive to ischemia (12, 14), was the important finding brought out by the light microscopic observation on ger-bils. The most striking lesion was the “reactive change”, confined to the H3 sector of the hippocampus (26). This change occurred only in the animals subjected to relatively slight ischemic insult and fully developed only upon recirculation. The neurons of the H3 sector were characterized by a peripheral shift of the nucleus whereas the voluminous cytoplasm showed a central chro-matolysis. The reversibility of these changes was evident from the almost normal appearance of the H3 sector in the animals sacrificed 1 week after the reestablishment of blood supply to the brain. It is thus evident that “reactive change” represents a cellular reaction to ischemia in which the neurons are capable of full recovery from an ischemic injury.

Keywords

Cresyl Violet Mongolian Gerbil Reactive Change Experimental Cerebral Ischemia Acta Neuropath 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Barron, K.D., Sklar, S. (1961): Response of lysosomes of bulbospinal motoneurons to axon section. Neurology (Minneap.) 11: 866–875.Google Scholar
  2. 2.
    Barron, K.D., Tunkboy, T.O. (1962): The histochemistry of acid phosphatase and thiamine pyrophosphatase during axon regeneration. Amer. J. Path. 40: 637–652.PubMedGoogle Scholar
  3. 3.
    Bubis, J.J., Fujimoto, T., Ito, U., Mršulja, B.J., Spatz, M. and Klatzo, I. (1976): Experimental cerebral ischemia in Mongolian gerbils V. Ultrastructural changes in H3 sector of the hippocampus. Acta neuropathol. (Berl.) 36: 285–294.CrossRefGoogle Scholar
  4. 4.
    Burstone, M.S. (1958): Histochemical demonstration of acid phosphatase. J. Nat. Cancer Inst. 21: 523–539.PubMedGoogle Scholar
  5. 5.
    Burstone, M.S. (1960): Histochemical demonstration of cytochrone oxidase with new amine reagent. J. Histo-chem. Cytochem. 8: 63–70.CrossRefGoogle Scholar
  6. 6.
    Burstone, M.S. (1961): Histochemical demonstration of phosphatases in frozen sections with naphthol AS-phos-phates. J. Histochem. Cytochem. 9: 146–153.PubMedCrossRefGoogle Scholar
  7. 7.
    Clendenon, N.R., Allen, N., Komatsu, T., Liss, L. and Gordon, W.A. (1971): Biochemical alterations in the anoxic-ischemic lesion of rat brain. Arch. Neurol. (Chic.) 25: 432–448.CrossRefGoogle Scholar
  8. 8.
    Friede, R.L. (1962): The cytochemistry of normal and reactive astrocytes. J. Neuropath, exp. Neurol. 21: 471–478.CrossRefGoogle Scholar
  9. 9.
    Friede, R.L. (1968): Mappings of oxydative enzymes in the brain. In: Pathology of the Nervous System, ed. J. Minckler, McGraw-Hill, New York, 306–320.Google Scholar
  10. 10.
    Gadamski, R., Eustachiewicz, R. (1974): Histochemical changes in medulla oblongata in rabbit caused by circulatory hypoxia (ischemia). Neuropath. Pol. 12: 603–615.Google Scholar
  11. 11.
    Hess, R., Scarpelli, D.G., Pearse, A.G.E. (1958): The cytochemical localisation of oxydative enzymes. Piridine nucleotide linked dehydrogenases. J. Biochem. Cytol. 4: 101–110.Google Scholar
  12. 12.
    Ito, U., Spatz, M., Walker, J.T. Jr., Klatzo, L. (1975): Experimental cerebral ischemia in Mongolian gerbils. I. Light microscopic observations. Acta Neuropath. (Berl.) 32: 209–223.CrossRefGoogle Scholar
  13. 13.
    Kahn, K. (1972): The natural course of experimental cerebral infarction in the gerbil. Neurology 22: 510–515.PubMedGoogle Scholar
  14. 14.
    Klatzo, I. (1975): Pathophysiological aspects of cerebral ischemia. The Nervous System, et. Tower, D.B., Raven Press, New York, Vol. I. The Basic Neurosciences 313–322.Google Scholar
  15. 15.
    Kozik, M. (1972): Doswiadczalny obrzek neuronu w badan histienzymatycznych. Neuropat. Pol. 10: 1–15.Google Scholar
  16. 16.
    László, I., Knyihar, E. (1975): Electron histochemistry of thiamine pyrophosphatase activity in the neuronal Golgi apparatus observed after axotomy and trans-neuronal deprivation. J. Neural Transmiss. 36: 123–141.CrossRefGoogle Scholar
  17. 17.
    Levine, S., Sohn, D. (1969): Cerebral ischemia in infant and adult gerbils. Relation to incomplete circle of Willis. Arch. Pathol. 87: 315–317.PubMedGoogle Scholar
  18. 18.
    Little, J.R., Kerr, F.W.L., Sundt, T.M.Jr. (1974): The role of lysosomes in production of ischemic nerve cell changes. Arch. Neurol. 30: 448–455.PubMedCrossRefGoogle Scholar
  19. 19.
    Maslinska, D. Thomas, E. (1975): Enzyme histochemical studies of “retrograde” reaction in motor neurons of immature rats. Acta Neuropath. (Berl.) 33: 317–323.CrossRefGoogle Scholar
  20. 20.
    Mossakowski, M.J. (1963): The activity of succinic dehydrogenase in the reactive glia. Acta Neuropath. (Berl.) 2: 282–290.CrossRefGoogle Scholar
  21. 21.
    Mršulja, B.J., Spatz, M., Walker, J.T. Jr., Klatzo, I. (1977): Histochemical investigation on the Mongolian gerbils brain during unilateral ischemia (submitted to Acta Neuropath. Berl.).Google Scholar
  22. 22.
    Novikoff, A.B., Essner, E. (1962): Pathological changes in cytoplasmic organelles. Fed. Proc. 21: 1130–1142.PubMedGoogle Scholar
  23. 23.
    Novikoff, A.B. (1963): Lysosomes in the physiology and pathology of cells. Contributions of staining methods. Ciba Foundation Symposium on Lysosomes, eds. A.V.S. de Reuck, M.P.L. Cameron, Little, Brown Comp. Boston, 36.CrossRefGoogle Scholar
  24. 24.
    Novikoff, P.M., Novikoff, A.B., Quintana, N. and Hauw, T.T. (1971): Golgi apparatus, GERL and lysosomes of neurons in rat dorsal root ganglia, studied by thick section and thin section cytochemistry. J. Cell Biol. 50: 859–886.PubMedCrossRefGoogle Scholar
  25. 25.
    Ogawa, K., Barrnett, R.J. (1965): Electron cytochemi-cal studies of succinic dehydrogenase and dehydro-nicotineamideadenine dinucleotide diaphorase activities. J. Ultrastruct. Res. 12: 488–508.PubMedCrossRefGoogle Scholar
  26. 26.
    Rose, M. (1931): Journal f. Psychol, u. Neurol. 43: 493–440. Tafeln 9–14.Google Scholar
  27. 27.
    Rubinstein, L.J., Klatzo, I., Wiquel, J. (1962): Histochemical observation on oxidative enzyme ectivity of glial cells in a local brain injury. J. Neuropath. exp. Neurol. 21: 116–136.PubMedCrossRefGoogle Scholar
  28. 28.
    Scarpelli, D.G., Pearse, A.G.E. (1958): Cytochemical localisation of succinic dehydrogenase in mitochondria. Anat. Rec. 132: 133–152.PubMedCrossRefGoogle Scholar
  29. 29.
    Sederholm, U. (1965): Histochemical localisation of esterases, phosphatases and tetrasolium reductases in the motor neurons of the spinal cord of the rat and the effect of nerve division. Acta physiol. scand. 65, Suppl. 256.Google Scholar
  30. 30.
    Spataro, J. (1966): Anoxic-ischemic encephalopathy of the rat brain. Exptl. Neurol. 16: 16–27.CrossRefGoogle Scholar
  31. 31.
    Spielmeyer, W. (1922): Histopathologic des Nervensystems. Springer, Berlin 74–79.Google Scholar
  32. 32.
    Van Harreveld, A., Trubatch, J. (1974): Reflex figures during asphyxiai rigidity. Expl. Neurol. 45: 161–173.CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1979

Authors and Affiliations

  • B. J. Mršulja
    • 1
    • 2
  • M. Spatz
    • 1
    • 2
  • I. Klatzo
    • 1
    • 2
  1. 1.Institute for Biological ResearchBelgradeYugoslavia
  2. 2.National Institute of Neurological and Communicative Disorders and StrokeNational Institutes of HealthBethesdaUSA

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